Actualización sobre encefalopatía hipóxica isquémica secundaria a asfixia perinatal

Abstract

Common intrapartum hypoxic-ischemic events include placental abruption, uterine rupture, umbilical cord prolapse, obstructed labor, misuse of oxytocin, and fetal infection, resulting in poor oxygenation and perfusion of vital organs. in the fetus and newborn. Perinatal asphyxia is characterized by hypoxia, hypercapnia, and metabolic acidosis, particularly hypoxia and ischemia with damage to vital organs. Hypoxic-ischemic injury to organs such as the skin, kidneys, liver, and heart is usually reversible. However, brain injury can lead to permanent neurological impairment. A hypoxic event can cause immediate damage in the case of cell necrosis, or belatedly in the case of neuronal cell apoptosis, which is responsible for a substantial amount of permanent brain damage after hypoxemia. perinatal asphyxia. Delayed cell death by apoptosis can be reduced with therapeutic interventions, current treatment for Hypoxic Ischemic Encephalopathy (HIE) mainly comprises therapeutic hypothermia to limit secondary energy failure. Therapeutic hypothermia has dramatically improved outcomes for infants with HIE, yet a considerable number of infants still die or sustain severe brain injury today. Therefore, continuous and precise study and research of updates and additional neuroprotective strategies is necessary.